The expression of vascular endothelial growth factor and its receptor in hematopoietic malignant cell lines HL-60 and Raji.
- Author:
Jin YE
1
;
Fu-Qiang LIU
;
Yi-Ping WU
Author Information
1. Department of Hematology, Beijing Tongren Hospital, Capital University of Medical Science, Beijing 100730, China. yej99@x263.net
- Publication Type:Journal Article
- MeSH:
Enzyme-Linked Immunosorbent Assay;
Extracellular Matrix Proteins;
analysis;
HL-60 Cells;
chemistry;
Humans;
Immunohistochemistry;
Lymphoma;
metabolism;
RNA, Messenger;
analysis;
Vascular Endothelial Growth Factor A;
analysis;
genetics;
Vascular Endothelial Growth Factor Receptor-1
- From:
Journal of Experimental Hematology
2003;11(4):376-380
- CountryChina
- Language:Chinese
-
Abstract:
In order to explore the effect of vascular endothelial growth factor (VEGF) in hematological malignancies, the expression of VEGF and its receptor was detected in HL-60 and Raji cells by reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme linked immunosorbent assay (ELISA) and immunohistochemistry. The results showed that VEGF-mRNA expressed in both HL-60 and Raji cells, and the mean VEGF concentrations in the cultural supernatant of both cell lines were significantly higher than that of normal peripheral blood mononuclear cell respectively. There was expression of VEGF-R (Flt-1) on the surfaces of both HL-60 and Raji cells. The research results demonstrated that VEGF-mRNA was expressed in hematopoietic malignant cell lines (HL-60 and Raji), and the corresponding protein was secreted into the extracellular microenvironment, the both cell lines expressed VEGF-R on the cell surface. VEGF affects not only vascular endothelial cells, but also leukemic and lymphoma cells themselves. It is suggested that an autocrine pathway of VEGF existed in the both cell lines other than the paracrine pathway. The autocrine pathway of VEGF works as basis of tumor invasion. In conclusion, to restrain expression of VEGF and its receptor may inhibit tumor growth, and helps to block the reciprocal loop between VEGF and endothelial cells, and decrease the tumor specialities of hyperproliferation, anti-apoptosis and invation, that may make the tumor more susceptible to chemotherapy.
